Thank you for another step in our quest for resolving this issue: whether we can measure the total senescent cell burden in a human, and from this determine whether this is a determinant in ageing. Whether it can be altered; and maybe how.
May I go a step at a time with you assertions?
“it is known senescent cells resist apoptosis” – by defninition
“senescence is triggered when telomeres reach a critical length and so stop dividing” Yes, but for other reasons too.
“this is what happens when we age” No, it occurs throughout our llifespan
“So given that senescent cells result from aging” As above, this is not true; it happens because cells age, not the host.
“they resist apoptosis” – no; most (all?) do not.
“then they will accumulate” – this is to be proved, not asserted.
“there is no alternative to them not accumulating” Yes there is. Apoptosis clears some (all?). This is the nub of the problem.
I’ve now spent quite some time reviewing many of the referenced research papers, both from your reference and others. Most of the papers quoted are themselves only reviews, not empirical research. Those that are empirical are focused on niche areas (mouse organs; cancers; lungs). Non are whole body senescent cell assays. I have failed to find any – such may exist, but I haven’t found them, and nobody I’ve read has quoted any.
The conjecture is not an unreasonable one: that we carry an increased amount of senescent cells as we age. But so what? We then have to prove that this causes a problem. Any problem such may cause is thought to be due to inflammation and/or a weakening of the immune system due to the latter being worn out by dealing successively with them. Hence, by implication, if either or both the inflammation and/or the immune system is healthy, then presumably the senescent cells are causing a problem – could that be due to them being mopped up? Or really being quiescent?
If there is anything to the senolytic idea – that there are compounds that clear the senescent cells – then why may that not already be being done by various aspects of one’s lifestyle, as perhaps indicated by reversing ageing problems (muscle-mass loss, inflammation, hand-grip, glossiness of hair a la the mice?)?
So what we need – and seems to be lacking, which is a shame, but hopefully someone’s on it, as without it nothing else can be done – is a biometric of total senescent burden. Present indications are that this will be difficult (Then, and only then, we can check all the assumptions being made: as Anat Biran st al notes in Quantitative identification of senescent cells in aging and disease - Biran - 2017 - Aging Cell - Wiley Online Library “ In vivo identification, quantification and characterization of senescent cells are challenging tasks that limit our understanding of the role of senescent cells in diseases and aging.” Before going to do that, with difficulty, in mouse tumours, fibrotic cells,, and tissues).
With such a metric, let’s call it Whole Senectic Cell Burden – WSCB – we can then, and only then, do the following:
On average do younger people have less WSCB than older people.
Does the WSCB continually rise as a person ages?
Does any lifestyle factor change the rate of WSCB in any one person?
Can WSCB be reduced?
Does WSCB correlate with other ageing biometrics?
Does reduction in WSCB improve other ageing biomarkers?
Etc.
There’s a long way to go before we make any sense of proposed synthetic Senolytics – which may not even better than lifestyle effects.
Best wishes! 
